Acceleration of Bone Repair in NOD-SCID Mice by Human Monoosteophils, Novel LL-37-Activated MonocytesReportar como inadecuado




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Background

An incomplete understanding of bone forming cells during wound healing and ectopic calcification has led to a search for circulating cells that may fulfill this function. Previously, we showed that monoosteophils, a novel lineage of calcifying-bone-forming cells generated by treatment of monocytes with the natural peptide LL-37, are candidates. In this study, we have analyzed their gene expression profile and bone repair function.

Methods and Findings

Human monoosteophils can be distinguished from monocytes, macrophages and osteoclasts by their unique up-regulation of integrin α3 and down-regulation of CD14 and CD16. Monoosteophils express high mRNA and protein levels of SPP1 osteopontin, GPNMB osteoactivin, CHI3L1 cartilage glycoprotein-39, CHIT1 Chitinase 1, MMP-7, CCL22 and MAPK13 p38MAPKδ. Monocytes from wild type, but not MAPK13 KO mice are also capable of monoosteophil differentiation, suggesting that MAPK13 regulates this process. When human monoosteophils were implanted in a freshly drilled hole in mid-diaphyseal femurs of NOD-SCID mice, significant bone repair required only 14 days compared to at least 24 days in control treated injuries.

Conclusion

Human derived monoosteophils, characterized as CD45+α3+α3β+CD34−CD14−BAP bone alkaline phosphatase− cells, can function in an animal model of bone injury.



Autor: Zhifang Zhang, John E. Shively

Fuente: http://plos.srce.hr/



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